1. Field of the Invention
The present invention relates generally to the fields of biochemistry and molecular oncology. More specifically, the present invention relates to uses of a novel cytokine, THANK, a TNF homologue that activates apoptosis, nuclear Factor-κB, and c-jun N-terminal kinase.
2. Description of the Related Art
In 1984, two homologous cytokines were reported to inhibit the growth of tumor cells specifically (1-7) and was named TNF-α and TNF-β (also called lymphotoxin). Since then over 15 members of this family have been identified, including FasL, CD29L, CD30L, CD40L, OX-40L, 4-1BBL, LT-β, TWEAK, TRAIL, RANKL/TRANCE, LIGHT, VEGI, and APRIL (8-16). At the amino acid sequence level, various members of the TNF family are 20-25% homologous to each other. Most members of this family play an important role in gene activation, proliferation, differentiation, and apoptosis. These ligands interact with the corresponding receptor, also members of the TNF receptor family, and activate the transcription factors NF-κB and AP1 (9, 17), a stress-activated protein kinase (c-jun N-terminal protein kinase, JNK), and a cascade of caspases.
The prior art is deficient in the lack of uses of a novel member of the TNF family, named THANK, for TNF homologue that activates apoptosis, NF-κB, and JNK. For example, the prior art is deficient in the lack of applications of THANK in inhibiting tumor growth and applications of THANK inhibitors in inhibiting the activation of NF-κB. The present invention fulfills this long-standing need and desire in the art.